Cortical Consequences of HIV-1 Tat Exposure in Rats are Enhanced by Chronic Cocaine

Author(s): Wesley N. Wayman, Lihua Chen, Amanda L. Persons, T. Celeste Napier

Journal Name: Current HIV Research
HIV and Viral Immune Diseases

Volume 13 , Issue 1 , 2015

Become EABM
Become Reviewer
Call for Editor


The life span of individuals that are sero-positive for human immunodeficiency virus (HIV) has greatly improved; however, complications involving the central nervous system (CNS) remain a concern. While HIV does not directly infect neurons, the proteins produced by the virus, including HIV transactivator of transcription (Tat), are released from infected glia; these proteins can be neurotoxic. This neurotoxicity is thought to mediate the pathology underlying HIVassociated neurological impairments. Cocaine abuse is common among HIV infected individuals, and this abuse augments HIV-associated neurological deficits. The brain regions and pathophysiological mechanisms that are dysregulated by both chronic cocaine and Tat are the focus of the current review.

Keywords: Addiction, calcium channels, Cav1.2, neuropathogenesis, prefrontal cortex.

Rights & PermissionsPrintExport Cite as

Article Details

Year: 2015
Published on: 11 March, 2015
Page: [80 - 87]
Pages: 8
DOI: 10.2174/0929867322666150311164504

Article Metrics

PDF: 56